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Background:Ultrasonographic gastrointestinal wall changes in dogs with acute pancreatitis (AP) are not well characterized in the literature. No detailed studies have described their prevalence, characteristics, distribution, or clinical relevance.Hypothesis/Objectives: Describe the prevalence of ultrasonographic gastrointestinal wall changes in a population of dogs with AP and evaluate for associations between the presence of gastrointestinal wall changes and clinical or clinicopathologica variables.Animals: Referral population of 66 client-owned dogs with AP.Methods: Retrospective search of clinical records to identify dogs with AP. Clinical variables, clinicopathological variables and ultrasonographic findings were reported using descriptive statistics. A binary logistic regression model was used to evaluate for associations between the presence of gastrointestinal wall changes and clinical or clinicopathological variables.Results: Sixty-six dogs were included. Forty-seven percent of dogs (95% confidence interval [CI], 35.0%-59.0%; n=31) with AP had ultrasonographic gastrointestinal wall changes. Gastrointestinal wall changes were most common in the duodenum and identified in 71% (n=22) of affected dogs. Of dogs with gastrointestinal wall changes, 74.2% (n=23) had wall thickening, 61.3% (n=19) had abnormal wall layering, and 35.5% (n=11) had wall corrugation. In the multivariable model, only heart rate remained an independent predictor of ultrasonographic gastrointestinal wallchanges (P=.02).Conclusions and Clinical Importance: Ultrasonographic gastrointestinal wall changes in this population of dogs with AP were common. Increased heart rate was the only independent predictor of gastrointestinal wall changes, which might imply more severe disease. Additional studies are required to elucidate whether ultrasonographic gastrointestinal wall changes reflect disease severity in AP.

Aims/hypothesis Diabetic cardiomyopathy (DCM) is a serious and under-recognised complication of diabetes. The first sign is diastolic dysfunction, which progresses to heart failure. The pathophysiology of DCM is incompletely understood but microcirculatory changes are important. Endothelial glycocalyx (eGlx) plays multiple vital roles in the microcirculation, including in the regulation of vascular permeability, and is compromised in diabetes but has not previously been studied in the coronary microcirculation in diabetes. We hypothesised that eGlx damage in the coronary microcirculation contributes to increased microvascular permeability and hence to cardiac dysfunction. Methods We investigated eGlx damage and cardiomyopathy in mouse models of type 1 (streptozotocin-induced) and type 2 (db/db) diabetes. Cardiac dysfunction was determined by echocardiography. We obtained eGlx depth and coverage by transmission electron microscopy (TEM) on mouse hearts perfusion-fixed with glutaraldehyde and Alcian Blue. Perivascular oedema was assessed from TEM images by measuring the perivascular space area. Lectin-based fluorescence was developed to study eGlx in paraformaldehyde-fixed mouse and human tissues. The eGlx of human conditionally immortalised coronary microvascular endothelial cells (CMVECs) in culture was removed with eGlx-degrading enzymes before measurement of protein passage across the cell monolayer. The mechanism of eGlx damage in the diabetic heart was investigated by quantitative reverse transcription-PCR array and matrix metalloproteinase (MMP) activity assay. To directly demonstrate that eGlx damage disturbs cardiac function, isolated rat hearts were treated with enzymes in a Langendorff preparation. Angiopoietin 1 (Ang1) is known to restore eGlx and so was used to investigate whether eGlx restoration reverses diastolic dysfunction in mice with type 1 diabetes. Results In a mouse model of type 1 diabetes, diastolic dysfunction (confirmed by echocardiography) was associated with loss of eGlx from CMVECs and the development of perivascular oedema, suggesting increased microvascular permeability. We confirmed in vitro that eGlx removal increases CMVEC monolayer permeability. We identified increased MMP activity as a potential mechanism of eGlx damage and we observed loss of syndecan 4 consistent with MMP activity. In a mouse model of type 2 diabetes we found a similar loss of eGlx preceding the development of diastolic dysfunction. We used isolated rat hearts to demonstrate that eGlx damage (induced by enzymes) is sufficient to disturb cardiac function. Ang1 restored eGlx and this was associated with reduced perivascular oedema and amelioration of the diastolic dysfunction seen in mice with type 1 diabetes. Conclusions/interpretation The association of CMVEC glycocalyx damage with diastolic dysfunction in two diabetes models suggests that it may play a pathophysiological role and the enzyme studies confirm that eGlx damage is sufficient to impair cardiac function. Ang1 rapidly restores the CMVEC glycocalyx and improves diastolic function. Our work identifies CMVEC glycocalyx damage as a potential contributor to the development of DCM and therefore as a therapeutic target. Graphical abstract

Heart rate variability (HRV) analysis measures the inter-beat interval variation of successive cardiac cycles. Measurement of these indices has been used to assess cardiac autonomic modulation and for arrhythmia identification in exercising horses.To report HRV indices during submaximal exercise, strenuous exercise and recovery, and explore relationships with clinical conditions (arrhythmias, lameness, equine gastric ulcer syndrome (EGUS), lower airway inflammation and upper respiratory tract obstructions (URTO) in Thoroughbred racehorses.Retrospective, observational cross-sectional study.One hundred and eighty Thoroughbred horses underwent a treadmill exercise test with simultaneous electrocardiographic (ECG) recording. Time-domain HRV indices (standard deviation of the R-R interval (SDRR); root mean square of successive differences (RMSSD)) were derived for submaximal and strenuous exercise and recovery segments. Clinical conditions (arrhythmia [during each phase of exercise], lameness, EGUS, lower airway inflammation and URTO) were assigned to binary categories for statistical analysis. Relationships between selected HRV indices and the clinical conditions were explored using linear regression models.During submaximal exercise, lameness was associated with decreased logRMSSD (B= -0.19 95% CI -0.31 to -0.06, P= 0.006) and arrhythmia was associated with increased logRMSSD (B= 0.31 95% CI 0.01-.608, P=0.04). During strenuous exercise, arrhythmia was associated with increased HRV indices (logSDRR B= 0.51 95% CI 0.40-0.62, P0.001; RMSSD B= 0.60 95% CI 0.49 to 0.72, P0.001). During recovery, arrhythmia was associated with increased HRV indices (logSDRR B= 0.51 95% CI 0.40-0.62 P0.001, logRMSSD B= 0.60 95% CI 0.49 to 0.72, P0.001).The main limitations of this retrospective study were that not every horse had the full range of clinical testing, therefore some horses may have had undetected abnormalities.The presence of arrhythmia increased HRV in both phases of exercise and recovery. Lameness decreased HRV during submaximal exercise.

Cardiac disease is an important cause of mortality in African wild dogs in human care. Vertebral heart scale (VHS) is a well-documented objective measure of cardiac size and is commonly used in domestic dogs. The VHS of 63 clinically healthy African wild dogs housed in zoological institutions was retrospectively calculated. Using the robust method of reference interval (RI) calculation, the RI for VHS in captive African wild dogs was 9.3-10.8. Echocardiographic measurements from 16 clinically healthy and 2 African wild dogs with preclinical dilated cardiomyopathy are reported. The cardiac biomarkers N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) were measured in a subset of African wild dogs. The median plasma NT-proBNP measurement was 845 pM/L (range 366-1,388) and the median serum cTnI measurement was 0.02 ng/ml (0.01-0.04). These data can be used for the assessment and identification of cardiac disease in this endangered species.

PetSavers is introducing a new feature called 'Meet the Researcher', which profiles veterinary scientists working on projects funded by PetSavers that aim to improve our understanding of diseases affecting companion animals. First to be interviewed in the series is Dr Melanie Hezzell who has been the recipient of several PetSavers’ grants.

Cardiac disease is commonly encountered in small animal practice. However, deciding whether an animal’s clinical signs are due to underlying cardiac disease or another process can be difficult. The topics discussed comprise B-type natriuretic peptide, troponins, combined measurements of NT-proBNP and cTnl, monitoring of digoxin therapy, assessment of nutritional deficiencies and genetic tests. This chapter also includes case examples.